Ebook ECG short rapid review for non-Cardiologists (edition 2.1): Part 1

(BQ) Part 1 book ECG short rapid review for non-Cardiologists presents the following contents: ECG basics, general physiological terms, sinus rhythms, atrio - Ventricular arrythmias. Invite you to consult.

ECG

Short Rapid Review

For Non-Cardiologists

Edition 2.1 (PocketBook)

Review Medicine with us at :

www.twitter.com/MedRx22

Dr CHIRAG NAVADIA

2013

**ABOUT BOOK **

Hello Dear Friends ,

I am Dr Chirag Navadia & Its my pleasure to present this ECG book as a compact version of other detailed ECG books This book is meant to be for all the Doctors , Nurses and Students around the world If you are curious to learn ECG Basics, then this is the book for you which is prepared after reviewing many other books out there These are some 50+ must know basic ECG with Interpretations, Clinical

Presentation, Etiologies & Managements

As this is a Review Book , It does not contain All Treatments

in Detail Emphasize has been made to include all clinically relevant important points Please See the index for more details about the topics in this book

I hope you will enjoy this book and will not regret your

purchase

Best Wishes For Your Brilliant Future

Sincerely

Dr Chirag Navadia

“Book is dedicated to my Parents , Friends, All College professors and Tutors of Kaplan Medical , USMLE First Aid , Dr Edward Goljan , Dr Hussain Sattar , Dr Najeeb Thanks for giving me most valuable knowledge of my

life “

Copyrights© 2013 Chirag Navadia

Certain ECG images were freely available on Internet & belongs to their Owner No part of this book may be reproduced in any form , by Photostat , microfilm , xerography or any other mean , or incorporated into any information retrieval system , electronic or mechanical , without the written permission of Chirag Navadia

TABLE OF CONTENTS

CHAPTER 1 : ECG BASICS………8

1.1 SHORT INTRODUCTION 8

1.2 CONDUCTION PATHWAY 11

1.3 BLOOD SUPPLY TO HEART 12

1.4 ACTION POTENTIALS 14

1.5 PHASES OF CARDIAC CYCLE 17

GENERAL PHYSIOLOGICAL TERMS 20

1.6 ECG RECORDING 22

1.8 BEST METHOD TO DETERMINE HEART RATE 29

1.9 TYPES OF ECG 30

1.10 STANDARD CHEST LEAD PLACEMENT OF ELECTRODES 33 1.11 CORONARY TERRITORY ON 12 LEAD ECG 35

1.12 ANALYSING THE RHYTHM 36

CHAPTER 2 : SINUS RHYTHMS………38

Normal ECG 38

Normal 12-Lead ECG 39

SINUS ARRYTHMIAS 40

SINUS BRADYCARDIA 41

SINUS TACHYCARDIA 43

SINUS PAUSE 45

CHAPTER 3 : ATRIO-VENTRICULAR ARRYTHMIAS ………47

ATRIAL TACHYCARDIA 47

MULTIFOCAL ATRIAL TACHYCARDIA 49

ATRIAL FLUTTER 50

ATRIAL FIBRILLATION 52

PREMATURE ATRIAL CONTRACTION 54

SUPRAVENTRICULAR TACHYCARDIA 56

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA 57

WANDERING ATRIAL PACEMAKER 60

CHAPTER 4 : VENTRICULAR ARRYTHMIAS……… 61

IDIOVENTRICULAR RHYTHM 61

ACCELETATED IDIOVENTRICULAR RHYTHM 62

VENTRICULAR TACHYCARDIA (MONOMORPHIC) 63

VENTRICULAR TACHYCARDIA (POLYMORPHIC) 65

VENTRICULAR FIBRILLATION 66

TORSADE DE POINTES 68

PULSELESS ELECTRICAL ACTIVITY 69

ASYSTOLE 71

CHAPTER 4 : HEART BLOCKS……….……….72

ATRIOVENTRICULAR BLOCKS (FIRST DEGREE BLOCK) 72

2 ND DEGREE AV BLOCK : MOBITZ TYPE I 74

2 ND DEGREE AV BLOCK : MOBITZ TYPE II 75

3 RD DEGREE AV BLOCK 77

SINOATRIAL BLOCK (SA BLOCK) 78

RIGHT & lEFT BUNDLE BRANCH BLOCKS 79

CHAPTER 5 : MYOCARDIAL INFARCTION………82

ECG CHANGE FROM DAY 1 TO YEAR LATER 86

ST SEGMENT CHANGES FROM ISCHEMIA TO MI 87

ST SEGMENT ELEVATION & DEPRESSION 88

INFERIOR WALL MI 91

ANTERIOR WALL MI 92

LATERAL WALL MI 93

CHAPTER 6 : JUNCTIONAL ARRYTHMIAS……….94

JUNCTIONAL RHYTHM 94

ACCELERATED JUNCTIONAL RHYTHM 95

JUNCTIONAL ESCAPE BEATS 96

WOLF-PARKINSON WHITE SYNDROME 97

PREMATURE JUCTIONAL CONTRACTIONS 98

SINGLE CHAMBER PACEMAKER RHYTHM - VENTRICULAR 99

SINGLE CHAMBER PACEMAKER RHYTHM - ATRIAL 100

DUAL CHAMBER PACEMAKER RHYTHM – ATRIAL & VENTRICULAR 100

CHAPTER 7 : PREMATURE VENTRICULAR CONTRACTIONS…………101

PVC : UNIFORM VS MULTIFORM 102

PVC : VENTRICULAR BIGEMINY VS TRIGEMINY 103

PVC : VENTRICULAR QUADRIGEMINY VS COUPLETS 104

CHAPTER 8 : MISCELLANEOUS……… 106

HYPERKALEMIA VS HYPOKALEMIA 106

HYPERCALCEMIA VS HYPOCALCEMIA 109

CHAPTER 9 : P & Q WAVE RELATIONSHIPS………112

P MITRALE/P SINISTROCARDIALE (MITRAL STENOSIS) 113

P PULMONALE (COR PULMONALE) 114

RIGHT ATRIAL ENLARGEMENT 114

LEFT ATRIAL ENLARGEMENT 115

MECHANISM OF Q WAVE 116

ACUTE PERICARDITIS 117

CARDIAC PHARMACOLOGY……….118

ANTI-ARRYTHMIC DRUGS 118

ANTIHYPERTENSIVE DRUGS 125

ANTIHYPERLIPIDEMIC DRUGS 128

NON PHARMACOLOGICAL TREATMENTS 130

References 132

CHAPTER 1 : ECG BASI CS

1.1 SHORT INTRODUCTION

Electrocardiogram (ECG)

The electrocardiogram is commonly used to detect abnormal heart rhythms and to investigate the cause of chest pains

What is an electrocardiogram?

An electrocardiogram (ECG) records the electrical activity of the heart The heart produces tiny electrical impulses which spread through the heart muscle to make the heart contract These impulses can be detected

by the ECG machine You may have an ECG to help find the cause of symptoms such as palpitations or chest pain Sometimes it is done as part of routine tests - for

example, before you have an operation

The ECG test is painless and harmless (The ECG machine records electrical impulses coming from your body - it does not put any electricity into your body.)

How is it done?

Small metal electrodes are stuck on to your arms, legs and chest Wires from the electrodes are connected to the ECG machine The machine detects and amplifies the electrical impulses that occur at each heartbeat and records them on to a paper or computer A few

heartbeats are recorded from different sets of electrodes The test takes about five minutes to do

Usually, more than two electrodes are used, and they can

be combined into a number of pairs (For example: left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs LA+RA, LA+LL, and RA+LL) The

output from each pair is known as a lead Each lead

looks at the heart from a different angle Different types

of ECGs can be referred to by the number of leads that are recorded, for example 3-lead, 5-lead or 12-lead ECGs (sometimes simply "a 12-lead")

A 12-lead ECG is one in which 12 different electrical signals are recorded at approximately the same time and will often be used as a one-off recording of an ECG, traditionally printed out as a paper copy Three- and 5-lead ECGs tend to be monitored continuously and viewed only on the screen of an appropriate monitoring device, for example during an operation or while being

transported in an ambulance There may or may not be any permanent record of a 3- or 5-lead ECG, depending

on the equipment used

What does an electrocardiogram show?

The electrodes on the different parts of the body detect electrical impulses coming from different directions within the heart There are normal patterns for each electrode Various heart disorders produce abnormal patterns The heart disorders that can be detected include :

- Abnormal heart rhythms If the heart rate is very fast, very slow, or irregular There are various types of irregular heart rhythm with

characteristic ECG patterns

- A heart attack (myocardial infarction), Whether it was recent or some time ago A heart attack causes damage to heart muscle, and heals with scar tissue These can be detected by abnormal ECG patterns

- An enlarged heart Basically, this causes bigger impulses than normal

All Other ECG are discussed in detail from Chapter 2 onwards

Limitations of the electrocardiogram

An ECG is a simple and valuable test Sometimes it can definitely diagnose a heart problem However, a normal ECG does not rule out serious heart disease For example, you may have an irregular heart rhythm that 'comes and goes', and the recording can be normal between

episodes Also, not all heart attacks can be detected by ECG Angina, a common heart disorder, cannot usually be detected by a routine ECG

Specialised ECG recordings sometimes help to

overcome some limitations For example:

Exercise ECG This is where the tracing is done when you

exercise (on a treadmill or exercise bike) This helps to assess the severity of the narrowing of the coronary arteries which causes angina

Ambulatory ECG This is where you wear a small

monitor which constantly records your heart rhythm This test records the electrical activity of your heart when you are walking about (ambulatory) and doing your normal activities It aims to detect abnormal heart rhythms that may 'come and go' The electrical activity is usually recorded for 24-48 hours

of time before the right and left ventricles (the two lower chambers of the heart)

The electrical impulse travels from the sinus node to the atrioventricular node (also called AV node), where

impulses are slowed down for a very short period & then allowed to continue down the conduction pathway via an electrical channel called as bundle of His into the

ventricles The bundle of His divides into right and left

pathways to provide electrical stimulation to the right

and left ventricles Each contraction of the ventricles

represents one heartbeat

1.3 BLOOD SUPPLY TO HEART

Image Courtesy : Principles of anatomy and physiology , 11e John Wiley &

Sons

The Heart is supplied by the Coronary arteries which

arises Behind the Aortic Valves 1) Left Coronary Artery

& 2) Right coronary artery

The left coronary artery is Further Devided into Left

circumflex artery and Left Anterior descending artery

aka Anterior Interventricular Branch

The Right Coronary Artery is Further Divided into Marginal Arteries, Nodal Arteries & Posterior

SA & AV Node Are Supplied by Branches of Left Coronary Artery in 10% Population called as Left Dominant Heart

Blood Vessel Area Supplied

Right Coronary Artery

Posterior Interventricular

Artery

To the Right atrium, Right ventricle and part of the left ventricle

Posterior Third of Interventricular Septum

Left Coronary Artery

Left anterior descending

artery To the Anterior wall of the left ventricle, Anterior 2/3rd

Interventricular septum, Bundle of His, Right bundle branch, and Left anterior fasciculus of the left bundle branch

Left Circumflex artery To the lateral walls of the

left ventricle, left atrium, and left posterior fasciculus

of the left bundle branch

Cardiac veins Collect blood from the

capillaries of the myocardium

Coronary sinus Returns blood to the right

atrium

1.4 ACTION POTENTIALS

Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane They are responsible for the generation of electrical impulses in the Heart

ACTION POTENTIAL IN FAST RESPONSE FIBRES

Fast Response Fibres : Cardiac Muscle , His-Purkinje System

Phase 0 : Phase of Depolarization : Depends on

number of Sodium Channels (Na+ coming into the cell)

which in turn depends on Resting membrane potential of cell Contraction occur during this phase (Atrial

depolarisation – P wave , Ventricular depolarization – first half of QRS complex) Class I antiarrythmics

(Procainamide, Quinidine, Disopyrimide) Blocks Phase 0

in fast response fibres

Phase I : Na+ channels are inactivated Overshoot

develops because of Potassium (K+) going out of cell & inward Chlorine current

Phase II : Plateau Phase : Balanced by slow Calcium

current going into the cell and Slow K+ going out of cell

Phase III : Repolarisation Phase : Delayed K+ rectifier

current rapidly increases and calcium channels get inactivated Atrial repolarization is not seen on ECG, It is believed to be hidden behind QRS complex , T wave indicates Ventricular repolarization Class III

antiarrythmics (Amiodarone , sotalol )slow down this phase

Phase IV : Return of membrane to resting potential

Maintained by Na+/K+ ATPase pump which send Sodium out of cell in exchange of Potassium Phase IV is flat in Fast fibres

ACTION POTENTIAL IN SLOW RESPONSE FIBRES

Slow Response Fibres : SA Node & AV Node

Phase 0 : Dependent on Calcium Channels (Not on

Sodium Channels With each depolarization SA node sends signal to contract the heart Class IV

antiarrythmics (Verapamil , Diltiazem) can slow or block this phase

Phase I & II is not present in SA & AV node

Phase III : Repolarisation phase , due to Potassium going

out of cell

Phase IV : Rising Slope (Not flat as in fast fibres) ,

referred to as Pacemaker current it’s due to inward Na+

& Ca++ current and outward K+ current (not well

understood yet) Class II (B blockers) & Class IV (Ca+ channel blockers) act on this phase and decreases heart rate

1.5 PHASES OF CARDIAC CYCLE

Image Courtesy : Hypocaffeinic.pbworks.com

5 Phases of Cardiac cycle are as follow :

Isovolumetric ventricular contraction : Volume in the

ventricles does not change during this phase

In response to ventricular depolarization, tension in the ventricles increases This increase in pressure within the ventricles leads to closure of the mitral and tricuspid

valves which give rise to the S1 heart sound The

pulmonic and aortic valves stay closed during the entire phase Ventricular Contraction is reflected by QRS complex on the ECG

The pressure during this phase gradually increases & when the pressure exceeds aortic and pulmonary

arterial pressure (ie at 80 mmHg), the aortic and

pulmonic valves open and the ventricles eject blood This

phase is called as Ejection Phase

Opening of Aortic & Pulmonary valves does not cause any heart sound

After an ejection phase the pressure inside ventricles start falling due to relaxation of ventricles When

ventricular pressure falls below the pressure in aorta and pulmonary artery, the Aortic and Pulmonic valves

closes This phase is called as isovolumetric relaxation

The closure of Pulmonary & Aortic valves give rise to S2 sound All valves are closed during this phase Atrial diastole occurs during this time and the blood fills the atria On the ECG it will be reflected by T Wave

Just on the side note remember that the pulmonic valve closes before the aortic valves which give rise to Split in

2nd heart sound which can be heard during inspiration

on auscultation Anything which delays Pulmonary valve closure will increase Splitting All Cardiac Sounds are discussed in more detail in our last section of Murmers

The phase of Rapid Ventricular filling : As the blood

continue to fill Atrium, The Atrial pressure exceeds ventricular pressure, which causes the mitral and

tricuspid valves to open, it will lead the Blood to flows passively from the atria into the ventricles

About 70% of ventricular filling takes place during this phase Sometimes S3 heart sound Is heard during this phase due to the rapid filling of ventricles example

(Normal in Youngs) Pathologically associated with

Dilated cardiomyopathy and some other pathologies

which will be discussed in Pathology section

After Rapid filling , Atrial systole will occur : Known as

the atrial kick, atrial systole (coinciding with late

ventricular diastole) It supplies the ventricles with the remaining 30% of the blood for each heartbeat & the

new cycle keeps going

Heart is Innervated mainly by Parasympathetic

(Vagus) Fibres & Sympathetic Fibres

Sympathetic Stimulation Increases Heart Rate The

Pain which arises during Angina travels through

Sympathetic Fibres to Spinal Cord segment T1-T5

Parasympathetic Stimulation Decreases Heart Rate

Sensory Fibres that Carry Afferent Limb of Cardiac Reflex Travel with Vagus Nerve

GENERAL PHYSIOLOGICAL TERMS

Preload is the load on Ventricular Muscles at the end of

Diastole It is determined mainly by Left Ventricular End Diastolic Volume & Left Ventricular End Diastolic

Pressure ie by Venous Return

Increase in Preload results in increase in Contractility which in turn increases Stroke Volume & thus increase in Ejection Fraction

A Rise in Pulmonary Capillary Wedge Pressure is

evidence of increased Preload on the Left Ventricle In Some Cases like Mitral Stenosis or Mitral Valve Prolapse

it is not a good index of Left Ventricular Preload

Stroke Volume is the amount of blood that heart pump

out with each beat It is affected by Contractility,

Afterload & Preload

Stroke Volume is Calculated as : SV = EDV (End Diastolic Volume) – ESV (End Systolic Volume)

EDV – Volume that is in the Left Ventricle after Diastole ESV – Volume That Remains in the Left Ventricle After Systole

Ejection fraction is the fraction of blood which heart

pumps out during 1 contraction which is usually 60% in healthy normal adult

Ejection Fraction = SV/End diastolic volume = ESV/EDV

Normal SV is 70 ml and EDV is 120 ml in 70kg man So if you calculate , it will come out to be 60%

Cardiac output = Heart Rate * Stroke Volume

So if the heart rate is 72 per minute , and stroke volume

is 70 ml , then Cardiac output in 1 minute = 5000ml or 5 Litres per minutes Chronic increase in preload is

Responsible for Dilated Cardiomyopathy

Ficks Principle says that : CO = Rate of O2 Consumption / Arterial O2 Content – Venous O2 Content

Mean Arterial Pressure is defined as Average arterial

pressure during since cardiac cycle It is calculated as : (i) MAP = Cardiac Output * Total Peripheral Resistance (ii) MAP = 2/3rd Diastolic Pressure + 1/3rd Systolic Pressure

Ex : If Mr John has Blood Pressure of 120/80 mmHg , His MAP will be – 2/3rd (80) + 1/3rd (120) = 92 mmHg

Pulse Pressure is merely the Difference between

Systolic Pressure and Diastolic Pressure, It is Calculated

as – PP = Systolic Pressure – Diastolic Pressure In Above Case, Mr John will have Pulse Pressure of 40mmHg

Afterload : The pressure AGAINST which heart will

work – determined by Peripheral Arterial resistance – Chronic increase in Afterload (eg Hypertension) will lead

to Left ventricular hypertrophy

From physiological formula : Blood flow = Pressure / Resistance (Q=P/R)

So if the resistance will increase, the blood flow will decrease and the heart will have to pump more amount

of blood against more resistance Chronically it will lead

to ventricular muscle hypertrophy

Five large blocks equal 1 second (5 ✕ 0.2) When

measuring or calculating a patient’s heart rate, a

6-second strip consisting of 30 large blocks is usually used The ECG strip’s vertical axis measures amplitude in

millimeters (mm) or electrical voltage in millivolts (mV) Each small block represents 1 mm or 0.1 mV; each large block, 5 mm or 0.5 mV

To determine the amplitude of a wave, segment, or interval, count the number of small blocks from the baseline to the highest or lowest point of the wave,

segment, or interval

1.7 INTERVALS AND SEGMENTS

RR

interval

It is the interval between a R wave

and the next R wave, Normal resting

heart rate is between 60 and 100

bpm

0.6s to 1.2sec

P wave

During Normal Atrial depolarization,

the main electrical vector is directed

from the SA node towards the AV

node and spreads from the right

atrium to the left atrium This turns

into the P wave on the ECG

For abnormal P waves see Right

Atrial Hypertrophy, Left Atrial

Hypertrophy, Atrial Premature

Beat, Hyperkalaemia

< 0.08s Height < 2.5mm

PR

interval

The PR interval is measured from

the beginning of the P wave to the

beginning of the QRS complex The

PR interval reflects the time the

electrical impulse takes to travel

from the sinus node through the AV

node and entering the ventricles

The PR interval is therefore a good

estimate of AV node function

For Short PR segment consider

Wolf-Parkinson-White syndrome or

Lown-Ganong-Levine syndrome

(other causes - Duchenne muscular

dystrophy, type II glycogen storage

disease (Pompe's), Hypertrophic

Obstructive CardioMyopathy)

For long PR interval see first degree

heart block and 'trifasicular' block

0.12 to 0.20s(3-

5 Small squares )

PR

segment

The PR segment connects the P wave

and the QRS complex

The impulse vector is from the AV

node to the bundle of His to the

bundle branches and then to the

Purkinje fibers This electrical

activity does not produce a

contraction directly and is merely

traveling down towards the

ventricles, and this shows up flat on

0.05 to 0.12s

the ECG The PR interval is more

clinically relevant

QRS

complex

The QRS complex reflects the rapid

depolarization of the right and left

ventricles The ventricles have a

large muscle mass compared to the

atria, so the QRS complex usually has

a much larger amplitude than the

P-wave

For Abnormally wide QRS consider

right or left bundle branch block,

ventricular rhythm, hyperkalaemia,

etc

0.08 to 0.12s (2-

3 small squares)

J-point

The point at which the QRS complex

finishes and the ST segment begins

It is used to measure the degree of

ST elevation or depression

N/A

ST

segment

The ST segment connects the QRS

complex and the T wave The ST

segment represents the period when

the ventricles are depolarized It is

isoelectric No elevation or

depression is normally seen

 Causes of elevation include

Acute MI (e.g anterior, inferior), left bundle branch block, normal variants (e.g

athletic heart, Edeiken

0.08 to 0.12s

pattern, high-take off), acute pericarditis

 Causes of depression

include myocardial ischemia, digoxin effect, ventricular hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block

T wave

The T wave represents the

repolarization of the ventricles The

interval from the beginning of the

QRS complex to the apex of the T

wave is referred to as the absolute

refractory period The last half of the

T wave is referred to as the relative

refractory period (or vulnerable

period)

Causes of tall T waves include

hyperkalaemia, hyperacute

myocardial infarction and left

bundle branch block

Causes of small, flattened or

inverted T waves are numerous and

include ischaemia, age, race,

hyperventilation, anxiety, drinking

iced water, LVH, drugs (e.g

digoxin), pericarditis, PE,

intraventricular conduction delay

(e.g RBBB)and electrolyte

disturbance.

0.16s

ST

interval

The ST interval is measured from the

J point to the end of the T wave

0.32s

QT

interval

The QT interval is measured from

the beginning of the QRS complex to

the end of the T wave A prolonged

QT interval is a risk factor for

ventricular tachyarrhythmias and

sudden death.Many drugs will

increase QT interval like :

amiodarone , antipshycotics ,

antidepressant , which increases the

risk to develop Torsade-de-pointes

Other Causes of long QT interval

- Romano Ward syndrome

(autosomal dominant)

- Jervill + Lange Nielson

syndrome (autosomal recessive) associated with sensorineural deafness

Up to 0.42s in heart rate of

60 bpm

U wave

The U wave is hypothesized to be

caused by the repolarization of the

interventricular septum It normally

has a low amplitude, and even more

often is completely absent

It always follows the T wave, and

also follows the same direction in

amplitude If it is too prominent,

suspect hypokalemia, hypercalcemia

or hyperthyroidism

J wave

The J wave, elevated J-point or

Osborn wave appears as a late delta

wave following the QRS or as a small

secondary R wave

It is considered pathognomonic of

hypothermia or hypocalcemia

1.8 BEST METHOD TO DETERMINE HEART RATE

Remember – 60 sec/min divided by 0.20 sec/large box =

1.9 TYPES OF ECG

1 : 12-lead ECG records electrical activity from 12 views

of the heart

2 : Single-lead or dual-lead monitoring provides

continuous cardiac monitoring

 The six precordial leads (leads V1 through V6) provide information about the heart’s horizontal plane

Leads I, II, and III

 Leads I, II, and III typically produce positive deflection on ECG tracings

 Lead I helps monitor atrial arrhythmias and hemiblocks

 Lead II commonly aids in routine monitoring and detecting of sinus node and atrial arrhythmias Normally , R wave is tallest in Lead ll

 Lead III helps detect changes associated with inferior wall myocardial infarction